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  1. 1

    المؤلفون: Jun-Ichi Yokota

    المصدر: Equilibrium Research. 57:254-270

    الوصف: Substantial advances in understanding of oculomotor function have come from basing models of the oculomotor system on the control system theory. In this model, vestibular nystagmus, OKN and OKAN are produced by combined activation of two important pathways. One process, called the direct-pathway, produced rapid changes in eye velocity. A second process (indirect pathway) causes only slow changes in eye velocity and contains a non-ideal integrator. This integrator, labeled a “velocity-storage integrator”, appears to hold or store activity related to slow phase eye velocity. Activities in the direct and indirect pathways combine to form the velocity signal (This signal drives the “velocity-to-position integrator”, which drives the oculomotor plant). The velocity storage mechanism serves as a focus for superimposing a variety of sensory inputs that signal motion and provide the central nervous system with a coordinate basis for interpreting continuous movement of the head relative to the environment. However, neural circuits underlying these mechanism are still unknown. The recent studies suggest that the velocity-storage integrator appears to lie in the vestibular nuclei (mainly medial vestibular nucleus, MVN), while the velocity-to-position-integrator is probably closely associated with the prepositus hypoglossi nuclei. The recent extracellular recording study shows that activities of “vestibular only” and “vestibular, plus saccade” units in the rostral MVN are likely to carry an eye velocity signal related to velocity storage.

  2. 2

    المؤلفون: Jun-Ichi Yokota, Eiji Sakata

    المصدر: Equilibrium Research. 55:275-282

    الوصف: The vestibulo-collic system senses the head position and movements three-dimen-sionally in space. In turn, it initiates activity in neck muscles that maintain an adequate head position to stabilize the angle of gaze.Surface electromyography (EMG) of neck muscles were recorded to determine responses of the vestibulo-collic system after acute, transient unilateral vestibular impairment resulted from the lidocaine anesthesia of the inner ear as a therapy for tinnitus. Nineteen patients treated by such therapy underwent recording before/after unilateral anesthesia. EMG recordings were obtained using surface electrodes on the sternocleidomastoid (SCM) and splenius (Sp) muscles in a lateral reclining position with the anesthetized ear upward. There were no remarkable changes in surface EMG activity of neck muscles in 3 normal subjects between supine and lateral positions before anesthesia. After anesthesia, EMG activity in the ipsilateral SCM was significantly increasing for 4-6 hours, while there were no remarkable changes in the contralateral SCM or the Sp on either side.Electrophysiological studies demonstrate that SCM motoneurons receive disynaptic excitatory inputs from contralateral vestibular canals and disynaptic inhibitory inputs from ipsilateral canals through the medial vestibulospinal tract (MVST). Taken together, results from this study suggest that increasing EMG activity of the ipsi-SCM could result from "disinhibition" of the inhibitory pathway from the ipsilateral, transiently suppressed vestibular activity due to inner ear local anesthesia.

  3. 3

    المصدر: Annals of the New York Academy of Sciences. 656:277-296

    الوصف: 1. Electrical stimulation of the nucleus of the optic tract (NOT) induced nystagmus and after-nystagmus with ipsilateral slow phases. The velocity characteristics of the nystagmus were similar to those of the slow component of optokinetic nystagmus (OKN) and to optokinetic after-nystagmus (OKAN), both of which are produced by velocity storage in the vestibular system. When NOT was destroyed, these components disappeared. This indicates that velocity storage is activated from the visual system through NOT. 2. Velocity storage produces compensatory eye-in-head and head-on-body movements through the vestibular system. The association of NOT with velocity storage implies that NOT helps stabilize gaze in space during both passive motion and active locomotion in light with an angular component. It has been suggested that "vestibular-only" neurons in the vestibular nuclei play an important role in generation of velocity storage. Similarities between the rise and fall times of eye velocity during OKN and OKAN to firing rates of vestibular-only neurons suggest that these cells may receive their visual input through NOT. 3. One NOT was injected with muscimol, a GABAA agonist. Ipsilateral OKN and OKAN were lost, suggesting that GABA, which is an inhibitory transmitter in NOT, acts on projection pathways to the brain stem. A striking finding was that visual suppression and habituation of contralateral slow phases of vestibular nystagmus were also abolished after muscimol injection. The latter implies that NOT plays an important role in producing visual suppression of the VOR and habituating its time constant. 4. Habituation is lost after nodulus and uvula lesions and visual suppression after lesions of the flocculus and paraflocculus. We postulate that the disappearance of vestibular habituation and of visual suppression of vestibular responses after muscimol injections was due to dysfacilitation of the prominent NOT-inferior olive pathway, inactivating climbing fibers from the dorsal cap to nodulouvular and flocculoparafloccular Purkinje cells. The prompt loss of habituation when NOT was inactivated, and its return when the GABAergic inhibition dissipated, suggests that although VOR habituation can be relatively permanent, it must be maintained continuously by activity of the vestibulocerebellum.